Within 8-12 weeks after "curative" resection of chemically induced autochthonous bowel tumors in Wistar/Furth (W/F) rats, 80% of operated animals develop local recurrence or second primary development. The present project will determine if, in the setting of minimal residual disease, specific facets of host antitumor response can be altered, favorably affecting this high incidence of tumor recurrence or second primary development: Cell surface antigens shown to be associated with rat bowel adenocarcinomas include "private" or idividually specific, common or "tissue type specific", "widespread" embryonic and gut-specific embryonal antigens. These markers have been demonstrated to be immunogenic during the induction and growth of primary tumors, and under certain conditions function in vivo as tumor rejection antigens. After clinically "curative" resection, rats will be treated with viable cells shown to possess "private", common or embryonal cell surface antigens associated with rat bowel tumors, or with non-crossreacting control sarcoma cells. Host immune responses will be followed serially by assaying cell mediated cytotoxicity (CMC), serum modification of CMC (blocking, "unblocking", potentiation) and complement dependent antibody mediated cytotoxicity. In vitro techniques will consist of "long-term" 51 Chromium assay and microcytoxicity assay (with visual counting), both of which are reproducible in this syngeneic tumor model. In vivo effects of treatment will be followed by repeated double contrast large bowel roentgenograms.